Coronary Blood Flow and Myocardial O2 Consumption in Hypertrophied Cardiac Muscle in Dogs

2015 ◽  
pp. 93-103 ◽  
Author(s):  
G. V. Marchetti ◽  
L. Merlo ◽  
O. Visioli
Keyword(s):  
Blood Flow ◽  
Cardiac Muscle ◽  
Coronary Blood Flow ◽  
O2 Consumption ◽  
Myocardial O2 Consumption

Effect of indomethacin on coronary blood flow during graded treadmill exercise in the dog

1984 ◽  
Vol 247 (3) ◽  
pp. H452-H458 ◽  
Author(s):  
X. Z. Dai ◽  
R. J. Bache
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arachidonic Acid ◽  
Coronary Blood Flow ◽  
Treadmill Exercise ◽  
Electromagnetic Flowmeter ◽  
Aortic Pressure ◽  
O2 Consumption ◽  
Vascular Response ◽  
Myocardial O2 Consumption

This study tested the hypothesis that metabolites of arachidonic acid may contribute to the coronary vascular response to physiological increases of myocardial O2 consumption that occur during exercise. Studies were performed in eight chronically instrumented dogs with electromagnetic flowmeter probes on the left circumflex coronary artery and aortic and coronary sinus catheters. Data were obtained at rest and during graded treadmill exercise during control conditions and after administration of the cyclooxygenase inhibitor indomethacin. During control conditions heart rate, aortic pressure, and coronary blood flow increased progressively during exercise; this was accompanied by a significant increase in myocardial O2 extraction, as evidenced by a decrease in coronary venous O2 tension (Po2) particularly during the first stage of exercise. Indomethacin (5 mg/kg iv) resulted in marked blunting of the coronary vasodilator response to intracoronary arachidonic acid in anesthetized open-chest dogs. After administration of indomethacin to awake dogs, resting heart rate, aortic pressure, and coronary venous Po2 were unaltered, and the response of these variables to exercise was not changed. The increase in coronary blood flow during exercise was also unchanged after indomethacin, so that the relationship between myocardial O2 consumption and coronary blood flow was unaltered by cyclooxygenase inhibition. Thus we were unable to demonstrate a significant effect of the prostaglandin system in mediating the coronary vascular response to exercise.

Reduced effect of phenylephrine on regional myocardial function and O2 consumption in experimental LVH

1995 ◽  
Vol 268 (3) ◽  
pp. H1202-H1207
Author(s):  
A. Roitstein ◽  
B. V. Cheinberg ◽  
J. Kedem ◽  
J. Tse ◽  
H. R. Weiss ◽  
...  
Keyword(s):  
Blood Flow ◽  
Radioligand Binding ◽  
Dissociation Constants ◽  
Regional Blood Flow ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
O2 Consumption ◽  
Adrenergic Stimulation ◽  
Alpha Adrenoceptor ◽  
Myocardial O2 Consumption

In a dog model of left ventricular hypertrophy (LVH) created by aortic valve plication, we examined the hypothesis that regional myocardial inotropic and metabolic responses to alpha-adrenergic stimulation would be diminished due to decreased alpha-adrenoceptor number. After systemic beta-adrenergic blockade, phenylephrine (PE, 5 micrograms.kg-1.min-1) was infused into the left anterior descending artery in eight LVH and nine control open-chest anesthetized dogs. The circumflex region served as control. In both regions, local segment work was calculated as the integrated products of force (miniature transducer) and segment shortening (ultrasonic crystals). Local myocardial O2 consumption was calculated from regional blood flow (microspheres) and O2 saturation (microspectrophotometry). A saturation radioligand binding assay was used to determine adrenoceptor number and affinity. In control animals in the treated region, PE increased work from 815 +/- 140 to 1,493 +/- 149 g.mm.min-1. In LVH, work was not significantly altered (688 +/- 142 vs. 730 +/- 149 g.mm.min-1). Regional blood flow was elevated in controls (81 +/- 10 to 141 +/- 24 ml.min-1.100 g-1) but was not changed in LVH (105 +/- 12 vs. 123 +/- 18 ml.min-1.100 g-1). In controls, but not in LVH, myocardial O2 consumption was almost doubled during PE infusion (6.2 +/- 0.9 vs. 12.0 +/- 2.1 ml O2.min-1.100 g-1). alpha-Adrenoceptor number and dissociation constants values were not different between control and LVH (15.7 +/- 2.8 vs. 16.4 +/- 2.7 fmol/mg protein; 13.2 +/- 3.4 vs. 16.9 +/- 4.3 nm, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Independent role of arterial O2 tension in local control of coronary blood flow

1990 ◽  
Vol 258 (5) ◽  
pp. H1388-H1394 ◽  
Author(s):  
J. F. Baron ◽  
E. Vicaut ◽  
X. Hou ◽  
M. Duvelleroy
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Perfusion Pressure ◽  
Rabbit Heart ◽  
Coronary Resistance ◽  
Heart Preparation ◽  
Myocardial O2 Consumption ◽  
O2 Delivery ◽  
Arterial Po2

The aim of this study of a blood-perfused isolated rabbit heart preparation was to differentiate the effects on coronary resistance of large changes in arterial O2 tension (arterial PO2 = 45-400 Torr) from the effects of variations in arterial O2 content or myocardial O2 delivery. Standard stored human blood was resuspended in Krebs-Henseleit buffer and was oxygenated to obtain normal PO2, high PO2, and low PO2. Hemoglobin concentrations were adjusted to obtain the same arterial O2 content (CaO2) for the three PO2s. In a first set of experiments, in which coronary blood flow (CBF) was free and adapted to a constant perfusion pressure, switching from control [138 +/- 17 (SE) Torr] to high PO2 blood (380 +/- 27 Torr) induced a significant decrease in CBF and myocardial O2 consumption (MVO2). Switching from control (125 +/- 3 Torr) to low PO2 blood (49 +/- 5 Torr) induced a significant increase in CBF and MVO2. In a second set of experiments, the switch from control (159 +/- 5 Torr) to high PO2 (389 +/- 32 Torr) was performed in a preparation in which CBF and consequently O2 delivery were constant. Under these conditions, the increase in perfusion pressure demonstrated that PO2 affected coronary resistance, even though the O2 delivery was constant. No significant change in myocardial performance was observed in any of these experimental procedures. These results show that arterial PO2 may affect coronary blood flow regulation independently of any mediation by the autonomic nervous system and of any associated changes in O2 content or O2 delivery.

Adrenergic vasoconstriction limits coronary blood flow during exercise in hypertrophied left ventricle

1991 ◽  
Vol 260 (5) ◽  
pp. H1489-H1494 ◽  
Author(s):  
R. J. Bache ◽  
D. C. Homans ◽  
X. Z. Dai
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Additional Contribution ◽  
Adrenergic Blockade ◽  
Myocardial O2 Consumption

This study was carried out to test the hypothesis that alpha-adrenergic vasoconstriction limits coronary blood flow (CBF) during exercise in the chronically pressure overloaded, hypertrophied left ventricle. Studies were performed in dogs in which left ventricular hypertrophy had been produced by banding the ascending aorta at 9 wk of age. Left circumflex coronary artery blood flow and myocardial O2 consumption (MVO2) were examined at rest and during treadmill exercise during control conditions, after selective alpha 1-adrenergic blockade with prazosin, and after nonselective alpha-adrenergic blockade with phentolamine. All studies were performed after beta-adrenergic blockade with propranolol. During control conditions CBF and MVO2 increased progressively during exercise, while coronary sinus O2 tension decreased. Neither prazosin nor phentolamine altered CBF at rest but, in comparison with control measurements, both agents significantly increased CBF during exercise and abolished the decrease in coronary sinus O2 tension that normally occurred during exercise. Both prazosin and phentolamine caused similar significant increases of MVO2 relative to the heart rate times systolic left ventricular pressure during exercise, indicating that the increased CBF produced by these agents enhanced MVO2. Similar findings after prazosin and phentolamine indicate that adrenergic restraint of CBF during exercise resulted principally from alpha 1-adrenergic vasoconstrictions with little additional contribution from postjunctional alpha 2-adrenergic mechanisms.

Regional oxygen consumption and supply in heart: effect of methoxamine-induced pressure rise

1981 ◽  
Vol 241 (3) ◽  
pp. H370-H375 ◽  
Author(s):  
H. R. Weiss
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Regional Differences ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
O2 Consumption ◽  
Regional Flow ◽  
Arterial Blood

The effect of raising arterial blood pressure 50 mmHg with methoxamine on regional left ventricular O2 supply and consumption was studied in 27 pentobarbital-anesthetized open-chest rabbits. Three groups of animals were studied: 1) control, 2) methoxamine infusion sufficient to raise pressure 50 mmHg, and 3) methoxamine infusion sufficient to raise pressure 50 mmHg with atrial pacing to maintain heart rate. Subepicardial (epi) and subendocardial (endo) O2 saturations were determined with a microspectrophotometric technique. Regional flow was determined with radioactive microspheres and regional O2 consumption by the Fick principle. In the control group, endo venous O2 saturation [31 +/- 3% (SE)] was lower than epi (42 +/- 2%). There were no significant regional differences in blood flow (avg 128 +/- 2 ml . min-1 . 100 g-1). With methoxamine when heart rate fell, there were no differences in regional flow or consumption when compared to control. During methoxamine infusion, when heart rate was maintained, there was higher coronary blood flow (361 +/- 52 ml . min-1 . 100 g-1) and O2 consumption (27 +/- 4 ml O2 . min-1 . 100 g-1). No regional differences, epi vs. endo, were found in this group. After a 50-mmHg pressure rise, the endo region of the left ventricle had an increased O2 consumption mediated by an increased coronary blood flow without a significant rise in O2 extraction, similarly to epi.

Persistent coronary vasodilation during long-term, supramaximal doses of adenosine

1984 ◽  
Vol 247 (5) ◽  
pp. H869-H873
Author(s):  
G. J. Crystal ◽  
H. F. Downey ◽  
F. A. Bashour
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Coronary Circulation ◽  
Muscle Blood Flow ◽  
Regional Myocardial Blood Flow ◽  
O2 Consumption ◽  
Coronary Vasodilation ◽  
Calculated Concentration ◽  
Myocardial O2 Consumption

Active and reactive hyperemias have been observed in the skeletal muscle circulation tachyphylactic to exogenous adenosine following 3-h supramaximal doses of the vasodilator. These findings failed to support a need for adenosine in metabolic control of skeletal muscle blood flow. The present study was conducted to determine if the coronary circulation also develops tachyphylaxis to adenosine while remaining sensitive to other metabolically linked vasodilator mechanisms. Experiments were conducted in eight pentobarbital-anesthetized, open-chest dogs whose blood flow in the left anterior descending coronary artery (LAD) was measured electromagnetically during 3-h infusion of adenosine into the LAD. Measurements of regional myocardial blood flow (radioactive microspheres), myocardial O2 consumption (Fick principle), and percent segment shortening (ultrasonic crystals) were also obtained. Adenosine was infused into the LAD at a rate of 27.0-72.0 mumol/min, depending on blood flow rate. Calculated concentration of adenosine in LAD blood averaged 0.484 +/- 0.111 mumol/ml, which was well in excess of that required for maximal coronary vasodilation. LAD blood flow averaged 21.5 +/- 2.2 ml/min during the preadenosine control condition. LAD blood flow after 3 h adenosine (123.3 +/- 23.0 ml/min) was not significantly different from that after 1-3 min adenosine (105.8 +/- 17.9 ml/min). There was no significant transmural variation in LAD blood flow during adenosine infusion. Adenosine had no significant effect on myocardial O2 consumption or percent segment shortening. Our results demonstrate persistent transmural vasodilation in the canine coronary circulation during long-term, supramaximal doses of adenosine and are consistent with a role for endogenous adenosine in maintenance of coronary vasodilation during sustained elevations in myocardial energy demands.

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